Schistosoma mansoni Larvae Do Not Expand or Activate Foxp3+ Regulatory T Cells during Their Migratory Phase.
Schistosoma mansoni Larvae Do Not Expand or Activate Foxp3+ Regulatory T Cells during Their Migratory Phase.
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DOI：
10.1128/iai.00408-15
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发表时间：
2015-10
影响因子：
3.1
通讯作者：
Taylor MD
中科院分区：
文献类型：
--
作者：
Redpath SA;van der Werf N;MacDonald AS;Maizels RM;Taylor MD
Foxp 3+调节性T（Treg）细胞通过控制破坏性免疫病理学和抑制保护性免疫在寄生虫感染期间抑制免疫应答中起关键作用。在曼氏血吸虫感染的专利阶段，Foxp 3 + Treg细胞被激活并抑制卵引起的Th 2应答，但很少有人知道它们在感染的早期预专利幼虫阶段的诱导和作用。我们在小鼠S.在C57 BL/6小鼠中，当幼虫寄生虫从皮肤迁移并通过肺途径到达肝和肠系膜血管时，可以观察到曼氏菌感染。与其他蠕虫感染相比，S.在感染的早期阶段，mansoni没有引起Foxp 3 + Treg细胞应答。我们发现Foxp 3 + Treg细胞的数量和比例在感染小鼠的肺、引流淋巴结和脾脏中保持不变。感染后Foxp 3 + Treg细胞的活化状态没有增加，如通过其CD 25、Foxp 3和Helios的表达所评估的。此外，感染不能诱导Foxp 3 + Treg细胞产生抑制性细胞因子白细胞介素10（IL-10）。相反，只有CD 4 + Foxp 3 − IL-4+ Th 2细胞在感染后表现出IL-10产生增加。这些数据表明Foxp 3 + Treg细胞在调节对S.曼氏血吸虫幼虫引起的初始免疫应答的特征。与对促进快速Foxp 3 + Treg细胞应答的其它寄生蠕虫感染的应答形成对比的是，对曼氏寄生虫的应答。
Foxp3+ regulatory T (Treg) cells play a key role in suppression of immune responses during parasitic helminth infection, both by controlling damaging immunopathology and by inhibiting protective immunity. During the patent phase of Schistosoma mansoni infection, Foxp3+ Treg cells are activated and suppress egg-elicited Th2 responses, but little is known of their induction and role during the early prepatent larval stage of infection. We quantified Foxp3+ Treg cell responses during the first 3 weeks of murine S. mansoni infection in C57BL/6 mice, a time when larval parasites migrate from the skin and transit the lungs en route to the hepatic and mesenteric vasculature. In contrast to other helminth infections, S. mansoni did not elicit a Foxp3+ Treg cell response during this early phase of infection. We found that the numbers and proportions of Foxp3+ Treg cells remained unchanged in the lungs, draining lymph nodes, and spleens of infected mice. There was no increase in the activation status of Foxp3+ Treg cells upon infection as assessed by their expression of CD25, Foxp3, and Helios. Furthermore, infection failed to induce Foxp3+ Treg cells to produce the suppressive cytokine interleukin 10 (IL-10). Instead, only CD4+ Foxp3− IL-4+ Th2 cells showed increased IL-10 production upon infection. These data indicate that Foxp3+ Treg cells do not play a prominent role in regulating immunity to S. mansoni larvae and that the character of the initial immune response invoked by S. mansoni parasites contrasts with the responses to other parasitic helminth infections that promote rapid Foxp3+ Treg cell responses.